B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation

Hyunkeun Song; Gabin Park; Yeong Seok Kim; Indo Hur; Hyunjin Kim; Jeoung Whan Ryu; Hyun Kyung Lee; Dae Ho Cho; In Hak Choi; Wang Jae Lee; Dae Young Hur

doi:10.1016/j.canlet.2008.02.067

B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation

Hyunkeun Song, Gabin Park, Yeong Seok Kim, Indo Hur, Hyunjin Kim, Jeoung Whan Ryu, Hyun Kyung Lee, Dae Ho Cho, In Hak Choi, Wang Jae Lee, Dae Young Hur

Research output: Contribution to journal › Article › peer-review

30 Citations (Scopus)

Abstract

B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.

Original language	English
Pages (from-to)	227-237
Number of pages	11
Journal	Cancer letters
Volume	266
Issue number	2
DOIs	https://doi.org/10.1016/j.canlet.2008.02.067
Publication status	Published - 2008 Aug 8
Externally published	Yes

Keywords

Apoptosis
B cell
B7-H4
EBV
Fas
FasL

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.canlet.2008.02.067

Cite this

B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation. / Song, Hyunkeun; Park, Gabin; Kim, Yeong Seok; Hur, Indo; Kim, Hyunjin; Ryu, Jeoung Whan; Lee, Hyun Kyung; Cho, Dae Ho; Choi, In Hak; Lee, Wang Jae; Hur, Dae Young.

In: Cancer letters, Vol. 266, No. 2, 08.08.2008, p. 227-237.

Research output: Contribution to journal › Article › peer-review

@article{767444cec4534857ab73cae64069511d,

title = "B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation",

abstract = "B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.",

keywords = "Apoptosis, B cell, B7-H4, EBV, Fas, FasL",

author = "Hyunkeun Song and Gabin Park and Kim, {Yeong Seok} and Indo Hur and Hyunjin Kim and Ryu, {Jeoung Whan} and Lee, {Hyun Kyung} and Cho, {Dae Ho} and Choi, {In Hak} and Lee, {Wang Jae} and Hur, {Dae Young}",

note = "Funding Information: This work was supported by the SRC/ERC program of MOST/KOSEF (Grant # R11-2005-017-02002-0) and MRC program of KOSEF grant funded by the Korean government (MOST) (R13-2007-023-00000-0), and the 2007 Inje University Research Grant.",

year = "2008",

month = aug,

day = "8",

doi = "10.1016/j.canlet.2008.02.067",

language = "English",

volume = "266",

pages = "227--237",

journal = "Cancer Letters",

issn = "0304-3835",

publisher = "Elsevier Ireland Ltd",

number = "2",

}

TY - JOUR

T1 - B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation

AU - Song, Hyunkeun

AU - Park, Gabin

AU - Kim, Yeong Seok

AU - Hur, Indo

AU - Kim, Hyunjin

AU - Ryu, Jeoung Whan

AU - Lee, Hyun Kyung

AU - Cho, Dae Ho

AU - Choi, In Hak

AU - Lee, Wang Jae

AU - Hur, Dae Young

N1 - Funding Information: This work was supported by the SRC/ERC program of MOST/KOSEF (Grant # R11-2005-017-02002-0) and MRC program of KOSEF grant funded by the Korean government (MOST) (R13-2007-023-00000-0), and the 2007 Inje University Research Grant.

PY - 2008/8/8

Y1 - 2008/8/8

N2 - B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.

AB - B7-H4 has an inhibitory effect on immune responses via the down-regulation of T cell-mediated immunity, but how the engagement of B7-H4 molecules by counter molecules affects the signaling mechanism of the B7-H4-expressing cells is poorly defined. In this study, we found that B7-H4 expression was enhanced on B cells infected with Epstein-Barr virus (EBV) and that triggering of these molecules induced apoptosis of EBV-transformed B cells. Engagement of B7-H4 initially increased intracellular level of ROS, which then induced the expression of FasL. Engagement of B7-H4 subsequently provoked Fas-mediated and caspase-dependent apoptosis in association with cytochrome c and AIF, and EndoG was released from the mitochondria on EBV-transformed B cells. These results suggest that B7-H4 may be a potential therapeutic target for EBV involved malignancy diseases.

KW - Apoptosis

KW - B cell

KW - B7-H4

KW - EBV

KW - Fas

KW - FasL

UR - http://www.scopus.com/inward/record.url?scp=45049087541&partnerID=8YFLogxK

U2 - 10.1016/j.canlet.2008.02.067

DO - 10.1016/j.canlet.2008.02.067

M3 - Article

C2 - 18417276

AN - SCOPUS:45049087541

VL - 266

SP - 227

EP - 237

JO - Cancer Letters

JF - Cancer Letters

SN - 0304-3835

IS - 2

ER -

B7-H4 reverse signaling induces the apoptosis of EBV-transformed B cells through Fas ligand up-regulation

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this